Purine nucleoside phosphorylase (PNP) under normal in vivo conditions catalyzes the phosphorolytic cleavage of the ribo- and deoxyribonucleosides of guanine and hypoxanthine to the corresponding sugar phosphate and guanine or hypoxanthine. In the absence of PNP, uric acid concentration is quite low while the concentration of certain nucleoside substrates of PNP such as (dGuo) in plasma and urine are elevated. dGuo is toxic towards lymphoblasts, however, T-cells are much more affected than are B-cells. Indeed, in patients with genetically acquired PNP deficiency, B-cell immunoglobulin production is normal or even elevated, but these patients are leukopenic and T-lymphocytic function is either totally lacking or is severely depressed. While uncontrolled PNP deficiency is obviously undesirable, there are many instances where controlled suppression of the immune system, and in particular controlled supression of T-cells, would be highly desirable such as in the treatment of T-cell leukemia, the suppresion of host-vs-graft response in organ transplant recipients, and the treatment of gout. Applicants have discovered a class of 9-purinyl phosphonic acid derivatives which are potent inhibitors of PNP and are thus useful as immunosuppressant agents.